Function of phagocytes and antibodies in juvenile periodontitis Localized juvenile periodontitis (LJP) is an early onset form of periodontal disease which affects 0.1-2.3% of otherwise healthy young people in the US. Actinobacillus actinomycetemcomitans (A.a.), a gram negative coccobacillus, has been strongly implicated as the causative pathogen of LJP. Although the mechanisms of pathogenesis of this disease have not been fully understood, many studies have suggested that a genetically predisposed defect might play a role in determining host susceptibility to A.a. infection. Initial studies on an inner city population of patients from Atlanta, GA., suggested that polymorphonuclear leukocytes (PMNs) from LJP patients were able to phagocytize, but not kill A.a.. Likewise LJP PMNs could be distinguished from controls by their relative resistance to Staphylococcus arueus leukocidin. On contrast. LJP PMNs from subjects in Orange County, NC are not discernibly different from their matched controls. The differences between the two geographic locations might be due to discrete environmental influences. Moreover, the questions of why LJP having such a unique clinical manifestations-bilateral symmetrical bone loss confined to the permanent first molars and/or incisors, and relative absence of clinical signs of inflammation? and why disease persisting while patients having a high level of antibody? are still unanswered. The purposes of this study are to examine the difference of host immune response between two LJP populations from two different areas, and to identify the unique aspect of A.a. LPS related to LJP's characterization. Blood samples from two LJP patient populations (Orange County and Charlotte, NC) will be collected, and the following assays conducted based on established methodology in this laboratory. 1) Phagocytosis and killing of A.a. by neutrophils from the patients; 2) Serum opsonization and facilitation of PMN-mediated killing; 3) Neutrophil chemotaxis; 4) Neutrophil susceptibility to Staphylococcus arueus leukocidin; and 5) Monocyte responsiveness to A.a. LPS challenge expressed by IL- I, TNF-a, and PGE2 production. LPS from A.a. will be extracted using two different methods (phenol-water method and phenol-chloroform-petroleum ether method) to determine if there are non-lipid A bound O-cetacean in A. a. LAPS. Non lipid A bound O-cetacean will consume antibody to A.a. and hence block effect of antibody to neutralize endotoxic activities of LAPS. Endotoxin-neutralizing-properties of antibodies from patient serum and rabbit anti-serum to A.a. will be evaluated by their inhibiting effect on the secretion of PGE2, IL-I, and TNF-a by monocytes from controls and patients.